Cellular crosstalk of mesangial cells and tubular epithelial cells in diabetic kidney disease

Abstract

Diabetic kidney disease (DKD) is a major cause of end-stage renal disease and imposes a heavy global economic burden; however, little is known about its complicated pathophysiology. Investigating the cellular crosstalk involved in DKD is a promising avenue for gaining a better understanding of its pathogenesis. Nonetheless, the cellular crosstalk of podocytes and endothelial cells in DKD is better understood than that of mesangial cells (MCs) and renal tubular epithelial cells (TECs). As the significance of MCs and TECs in DKD pathophysiology has recently become more apparent, we reviewed the existing literature on the cellular crosstalk of MCs and TECs in the context of DKD to acquire a comprehensive understanding of their cellular communication. Insights into the complicated mechanisms underlying the pathophysiology of DKD would improve its early detection, care, and prognosis.

The role of long non‐coding RNAs in the development of diabetic kidney disease and the involved clinical application

“…Diabetic kidney disease (DKD) is one of the major microvascular complications of DM 7 and is the leading cause of end‐stage renal diseases (End‐stage renal disease) 8 . Statistics show that DKD affects over 40% of DM patients and presents a significant global healthcare challenge 9 . The pathophysiology of DKD is multifactorial and involves various renal targets being damaged under hyperglycaemic (HG) conditions.…”